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. 2011 Jul 12;105(3):382–392. doi: 10.1038/bjc.2011.244

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Copyright © 2011 Cancer Research UK

This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material.If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/.

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Growth inhibitory effects of treatment with selective MEK inhibitors in parental and TKI-R CALU-3 cancer cells. MTT cell proliferation assays were performed in parental lung adenocarcinoma CALU-3 cells (P) and in their TKI-R derivatives (ERL-R, GEF-R, VAN-R and SOR-R), treated for 3 days with the indicated concentrations of each of two selective MEK inhibitors, MSC19363669B (A) or selumetinib (C). Results represent the average (±s.d.) of three separate experiments, each performed in quadruplicate. Western blotting analysis of MEK and MAPK activation following treatment with the indicated concentration of each of two selective MEK inhibitors, MSC19363669B (B) or selumetinib (D) on TKI-R CALU-3 and on parental cell line (E). β-Actin was included as a loading control.